ERK

CMIT/MIT (14.5% in water) (CMI/MI) is a mixture of CMIT and MIT, and is also a preservative and skin sensitizer. CMIT/MIT (14.5% in water) increases the levels of phosphorylated ERK1/2, p38, JNK1/2, p53, p21 and Bax, decreases the level of Bcl-2, and activates the Nrf-2/HO-1 signaling pathway. CMIT/MIT (14.5% in water) increases LDH release and lipid peroxidation levels, impairs antioxidant defense capacity, promotes pro-inflammatory cytokine release, induces apoptosis, triggers cell cycle arrest, exhibits neurotoxicity in neuroblastoma cells, and causes dysregulation of Th2/Th17 immune responses. CMIT/MIT (14.5% in water) can be used in studies related to allergy, atopic dermatitis and lung injury.

CHPG is a selective mGluR5 agonist, and attenuates SO₂-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells. CHPG protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways.

Lidocaine (Lignocaine) hydrochloride hydrate inhibits sodium channels involving complex voltage and using dependence. Lidocaine hydrochloride hydrate decreases growth, migration and invasion of gastric carcinoma cells via up-regulating miR-145 expression and further inactivation of MEK/ERK and NF-κB signaling pathways. Lidocaine hydrochloride hydrate is an amide derivative and has potential for the research of ventricular arrhythmia.

AG126 is a tyrosine kinase inhibitor, can inhibit the phosphorylation of ERK1 and ERK2 at 25-50 μM. AG126 can be used in meiosis, mitosis, and postmitotic research.

Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway. Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM_2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes.

Gambogic amide is a potent and selective agonist of TrkA and also induces its tyrosine phosphorylation and activation of downstream signaling, including Akt and MAPK. Gambogic amide specifically interacts with the cytoplasmic juxtamembrane domain of the TrkA receptor and triggers its dimerization, leading to activation. Gambogic amide has neuroprotective activity preventing glutamate-induced neuronal cell death. Gambogic amide has improved efficacy in a transient middle cerebral artery occlusion model of stroke and could be used to study neurodegenerative diseases and stroke.

Prexigebersen sodium is an antisense oligonucleotide designed to inhibit protein synthesis of Grb2 (growth factor receptor bound protein 2).

Mogrol is a biometabolite of mogrosides, and acts via inhibition of the ERK1/2 and STAT3 pathways, or reducing CREB activation and activating AMPK signaling.

XMD17-109 is a novel, specific ERK-5 inhibitor, with an IC₅₀ of 162 nM.

Ganglioside GM1 is a type of glycosphingolipid, mainly found on the cell membranes of the central nervous system of vertebrates. Ganglioside GM1 exerts neuroprotective effects by reducing excessive activation of NMDAR, activating TrkA and ERK1/2, and inhibiting oxidative stress and cell apoptosis and autophagy. Ganglioside GM1 can be used in the research of diseases such as traumatic brain injury, Parkinson's disease, Alzheimer's disease, and Huntington's disease.

6'-Sialyllactose promotes the growth of beneficial bacteria (such as Bifidobacterium and lactobacillus) and inhibits the proliferation of harmful bacteria. 6'-Sialyllactose exhibits anti-inflammatory and anti-angiogenic activities. 6'-Sialyllactose promotes the muscle health.

PDRN (Polydeoxyribonucleotide) is a deoxynucleotide polymer mainly derived from the sperm of rainbow trout or salmon. PDRN inhibits pro-inflammatory factors and promotes VEGF expression via the cAMP-PKA pathway by activating the adenosine A_2A receptor (A_2AR), thereby driving angiogenesis and collagen deposition in fibroblasts. Degradation products of PDRN provide DNA raw materials for proliferating cells through the salvage synthesis pathway, accelerating re-epithelialization. PDRN reduces melanin synthesis and cell apoptosis by upregulating ERK/AKT phosphorylation and inhibiting the activities of MITF and tyrosinase, and resists skin aging by attenuating nuclear autophagy and blocking the interaction between LC3-SIRT1. PDRN is mainly used for wound repair, post-aesthetic surgery recovery and anti-aging research.

Fenoprofen (LILLY-53858) Calcium hydrate is a nonsteroidal anti-inflammatory agent (NSAID) and inhibits cyclooxygenase (COX). Fenoprofen Calcium hydrate is a melanocortin receptors (MCRs) positive allosteric modulator (PAM). Fenoprofen Calcium hydrate also increases ERK1/2 activation in HEK293T cells. Fenoprofen Calcium hydrate has anti-arthritic activities and can be used for the study of rheumatoid arthritis and osteoarthritis.

TriDAP dihydrochloride (L-Ala-γ-D-Glu-meso-diaminopimelic acid dihydrochloride) is a NOD1 agonist with a K_d value of 34.5 μM. TriDAP dihydrochloride enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP dihydrochloride downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP dihydrochloride decreases IκBα levels and increases p65 levels. TriDAP dihydrochloride induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP dihydrochloride increases the RANKL/OPG ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP dihydrochloride can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection.

Arundic Acid is an orally effective astrocyte function modulator and neuroprotective agent. Arundic Acid increases the expression and function of the astrocytic glutamate transporter EAAT1 by activating the ERK, Akt and NF-κB pathways. Arundic Acid attenuates retinal ganglion cell death in a normal-tension glaucoma model. Arundic Acid exerts neuroprotective effects in a mouse model of Parkinson's disease. Arundic Acid is a S100β protein synthesis inhibitor that prevents neurological deficits and brain tissue damage after intracerebral hemorrhage in rats. Arundic Acid downregulates neuroinflammation and astrocytic dysfunction after status epilepticus in immature rats. Arundic Acid is applicable to research related to Parkinson's disease, cerebral ischemia, glaucoma, intracerebral hemorrhage and epilepsy.

Isorhamnetin-3-O-glucoside is an orally active natural compound. Isorhamnetin 3-O-glucoside increases P-ERK, ERK, P-Akt (Ser473), P-PI3K, and PDX-1. Isorhamnetin 3-O-glucoside downregulates C/EBPα and inhibits lipase. Isorhamnetin 3-O-glucoside reduces lipids and inhibits obesity.

TRV055 (TRV120055) is a G protein-biased agonist of angiotensin II type 1 receptors (AT1Rs). TRV120055 induces fibroblast proliferation, overexpression of collagen I and α-SMA, and stress fibre formation in human cardiac fibroblasts. TRV055 activates AT1 receptor/Gαq-mediated signaling pathways, upregulates TGF-β1 and p-ERK1/2. TRV055 induces collagen secretion in adult rat myofibroblasts at a level comparable to Ang II. TRV055 can be used to study the role of G protein-biased signaling of AT1Rs in regulating fibrotic responses^[1]

Cenupatide (UPARANT) is a uPAR and FPR antagonist with anti-angiogenic, anti-inflammatory, and vascular barrier regulatory activities, as well as high stability and resistance to enzymatic degradation in blood/plasma. Cenupatide blocks the uPAR-FPR interaction, reduces VEGF-induced phosphorylation levels of AKT, VEGFR-2, STAT3, JNK, p38 MAPK, ERK1/2, and NF-κB p65, and inhibits αvβ3 integrin activation. Cenupatide suppresses endothelial cell migration, invasion, tube formation, and angiogenic signaling pathways, restores tight junctions and blood-retinal barrier integrity, reduces pro-inflammatory marker levels, and inhibits apoptosis. Cenupatide reduces retinal neovascularization, renal fibrosis, and vascular leakage, and restores visual function in preclinical models. Cenupatide is applicable to research related to retinopathy, diabetic complications, ocular diseases, cancer, and inflammatory diseases.

ERK5-IN-2 is an orally active, sub-micromolar, selective ERK5 inhibitor with IC₅₀s of 0.82 μM, 3 μM for ERK5 and ERK5 MEF2D, respectively. ERK5-IN-2 does not interact with the BRD4 bromodomain. ERK5-IN-2 suppresses both tumor xenograft growth and basic fibroblast growth factor (bFGF) driven Matrigel plug angiogenesis.

CHPG sodium salt is a selective mGluR5 agonist, and attenuates SO₂-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells. CHPG sodium salt protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways..